The treatment of central nervous system diseases, such as post-traumatic stress syndrome, resulting mostly from traffic accidents, stroke, spinal cord injury, etc., has typically resorted to surgical operations and physical modalities while waiting expectedly for the advent of effective therapeutic drugs. The mechanism of recovery from injury commonly found in the diseases induced by central nervous system injury is the formation of fibrotic-glial scars. The fibrotic-glial scars serve as a kind of physiological barrier which act to confine inflammatory activity to the injured tissues so as to minimize the secondary injury induced by inflammation. In the art, accordingly, controlling the formation of fibrotic-glial scars is recognized as playing an important role in the treatment and/or improving the prognosis of central nervous system injury-induced diseases.
AKAP12 (A-Kinase anchoring protein 12), a member of the scaffolding protein family and present within cells, is known to be down-regulated in response to the activation of oncogenes such as src or ras. Particularly in association with a β-adrenergic receptor, PKC, PKA, and F-actin, AKAP12 is involved in signaling pathways. Also, it is reported that AKAP12 participates in cell migration, mitosis, and the regulation of blood barrier formation and apoptosis. However, nowhere have the roles and/or functions of AKAP12 in the formation of fibrotic-glial scars been mentioned in previous documents, thus far.